https://orcid.org/0000-0002-7939-3489
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ABSTRACT
Background
There is little evidence to guide the perioperative management of patients on a direct oral anticoagulant (DOAC) in the absence of a last known dose. Quantitative serum titers may be ordered, but there is little evidence supporting this.
Aims
This multi-center retrospective cohort study of consecutive surgical in-patients with a DOAC assay, performed over a five-year period, aimed to characterize preoperative DOAC assay orders and their impact on perioperative outcomes.
Materials and methods
Patients prescribed regular DOAC (both prophylactic and therapeutic dosing) with a preoperative DOAC assay were included. The DOAC assay titer was evaluated against endpoints. Further, patients with an assay were compared against anticoagulated patients who did not receive a preoperative DOAC assay. The primary endpoint was major bleeding. Secondary endpoints included perioperative hemoglobin change, blood transfusions, idarucizumab or prothrombin complex concentrate administration, postoperative thrombosis, in-hospital mortality and reoperation. Adjusted and unadjusted linear regression models were used for continuous data. Binary logistic models were performed for dichotomous outcomes
Results
1065 patients were included, 232 had preoperative assays. Assays were ordered most commonly by Spinal (11.9%), Orthopedics (15.4%), and Neurosurgery (19.4%). For every 10 ng/ml increase in titer, the hemoglobin decreases by 0.5066 g/L and the odds of a preoperative reversal increases by 13%. Compared to those without an assay, patients with preoperative DOAC assays had odds 1.44× higher for major bleeding, 2.98× higher for in-hospital mortality and 16.3× higher for receiving anticoagulant reversal.
Conclusion
A preoperative DOAC assay order was associated with worse outcomes despite increased reversal administration. However, the DOAC assay titer can reflect the patient’s likelihood of bleeding.
Declaration of financial/other relationships
R Mahajan has served on the advisory board of Abbott and Medtronic. The University of Adelaide reports receiving on behalf of Dr Mahajan lecture and/or consulting fees from Abbott, Bayer, Biotronik, Medtronic, and Pfizer. The University of Adelaide reports receiving on behalf of Dr Mahajan research funding from Abbott, Bayer, and Medtronic. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.
Author contributions
The authors confirm their contribution to the paper as follows – study conception and design: B Stretton. J Kovoor, S Bacchi, S Gluck, A Vanlint, M Afzal, C Ovenden, A Gupta, R Mahajan, S Edwards, Y Brennan, J Boey, B Reddi, G Maddern, M Boyd. Data collection: B Stretton, J Kovoor, S Bacchi, A Booth, and S Gluck. Investigation, analysis, and interpretation of results: B Stretton, J Kovoor, D Bacchi, S Gluck, A Vanlint, M Afzal, C Ovenden, A Gupta, R Mahajan, S Edwards, Y Brennan, J Boey, B Reddi, G Maddern, and M Boyd. Manuscript preparation: B Stretton, J Kovoor, S Bacchi, A Booth, S Gluck, A Vanlint, M Afzal, C Ovenden, A Gupta, R Mahajan, S Edwards, Y Brennan, J Boey, B Reddi, G Maddern, M Boyd. Supervision: R Mahajan, Y Brennan, J Boey, B Reddi, G Maddern, and M Boyd. All authors reviewed the results and approved the final version of the manuscript.